Topic might be old and tired but I just wanted to know what others are doing I'm trying to help my mother.
Quote:The novel hypothesis is, if when administered properly 5-HTP has no side effects, then there is no justifiable reason to not substitute 5-HTP for carbidopa. The current medical care standard not only fails to recognize the vast array of carbidopa-induced B6 deficiency issues, it is actively facilitating permanent electrical damage progression and inducing reversible PD symptom deterioration every day carbidopa is prescribed and taken.
Following the conclusion of our investigation the decision has been made to retract the published article. The authors did not provide the requested IRB and informed consent information relating to this study and it was determined the study did not meet the ethical publication requirements for research involving human subjects. These requirements are based on guidelines issued by the World Medical Association and the International Committee of Medical Journal Editors. Additionally, the authors did not provide the study protocols, raw data and other study documents relating to this study as requested. Given our concerns about the standard of research ethics, competing interests and that the authors have not supplied the information we requested to verify and validate the reported findings, the editor has determined the article should be retracted.
Always shocking to see people wanting to enrich themselves over the suffering of others. Too bad this still underexposed phenomenon has become somewhat "tainted" by this and we still have to wait for further thorough reliable research. 🍀
Beware B6. 200 mg is toxic to nerves -- even though most B complex pills I see seem to have 100mg. Also, B6 counteracts the workings of the Carbidopa in Carbidopa Levadopa -- which works to steer most of the dopamine brain food (CL) to your brain where it will do you good.
Link to long (very long) essay by biochemist in which he describes the backsliding effect on him of B6 -- when he started taking a B complex. Easiest part to read way at the end.
There are problems with the paper you quoted as Hikoi pointed out. But it contains a blinding truth: carbidopa introduces 'a vast array of carbidopa-induced B6 deficiency issues.'
You can deal with the issue by -
[1] Avoiding Levodopa/Carbidopa and going the Mucuna Pruriens route with green tea as a substitute for Carbidopa to get around the issue of the peripheral use of Levodopa. (Hardly any one here uses 5HTP)
[2] Supplement with the desired form of B6 (P5P) in the amounts and timeframe stated by park_bear .
Too many on this forum ignore the importance of Vitamin B6 and its involvement in over 150 critical biochemical reactions. Do not therefore ignore Marty Hinz insight: there is a price to pay if you do.
yes but “Houston we have a problem” one more. Prolonged use of Benserazide and carbidopa reduces b3 NA with all the consequences of the case (most important in my opinion). I quote:
“Niacin depletion in Parkinsonian patients treated with L-dopa, benserazide and carbidopa.
1. Benserazide and carbidopa, decarboxylase inhibitors used in the treatment of Parkinson's disease, have been shown to inhibit the enzyme kynurenine hydrolase in rat and mouse liver. This results in reduced synthesis of nicotinamide coenzymes from tryptophan, and hence an increased reliance on dietary niacin. 2. Pellagra might be expected as a result of this inhibition of endogenous synthesis of nicotinamide nucleotides, but has not been reported in patients treated with either drug. 3. The urinary excretion of N1-methyl-nicotinamide, a product of nicotinamide nucleotide metabolism, is considerably reduced in patients treated with dopa alone or in combination with an inhibitor of peripheral dopa decarboxylase, to as low as 40% of the control value. This means that many of these patients could be classified as' at risk'of niacin deficiency, even if not frankly deficient. 4. Patients treated with dopa plus a decarboxylase inhibitor, but not those treated with dopa alone, also show a reduced excretion of xanthurenic acid, and an increased excretion of kynurenine, as would be expected after inhibition of the kynurenine pathway, and possibly indicative of marginal vitamin B6 deficiency. "
however In my poor opinion I would not use 5-HTP because I already find it difficult to balance C / L let alone, but I would supplement C / L with B vitamins and that's it.
... and 'pray tell' Gioc how significance is the issue of inhibition/dysregulation of the kynurenine pathway ?
According to Wiki, this (B6 & B2 dominated pathway) is being investigated for the role 'dysregulation of this pathway [plays] in aging, neurodegenerative diseases, mental disorders, and chronic fatigue syndrome.'
Here is Simon from Science of Parkinson's for a tight PD focus
In today’s post, we will delve into what the kynurenine pathway is, explore how it relates to Parkinson’s, and discuss some of the approaches soon heading for the clinic.
Brava matcharoe! On the road to knowledge many doors must be opened, but the first of all is “the consideration of not knowing“. Without opening this door, knowledge is precluded.
Leave this sad thought to itself. Obviously what you don't know no one else knows otherwise they would be healed. 😂 . I apologize to Marimar for the out topic.
Thanks CaseyInsights, this is "proper data importance assessment by purpose" - very appropriate and thorough.
In a sea of data, where every drop is equal to the other when there is a need for Knowledge that is theoretical, practical and results certainty, few people are up to it.
Three of them are featured in this thread CaseyInsights, Park Bear, Hikoi.
what troubles me (besides the big words that I barely understand) is if a B supplement is necessary or helps why didn't Prof Lees suggest it when I was his patient. Admittedly it was 30 years after that paper was published.
and why are you telling me? You should ask him who did and wrote this research. Also because there have been more recent confirmations of this vitamin B3 deficiency, see here:
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